Rationale: Few studies have examined associations between longterm exposure to fine particulate matter (PM 2.5 ) and lung function decline in adults.Objectives: To determine if exposure to traffic and PM 2.5 is associated with longitudinal changes in lung function in a population-based cohort in the Northeastern United States, where pollution levels are relatively low.Methods: FEV 1 and FVC were measured up to two times between 1995 and 2011 among 6,339 participants of the Framingham Offspring or Third Generation studies. We tested associations between residential proximity to a major roadway and PM 2.5 exposure in 2001 (estimated by a land-use model using satellite measurements of aerosol optical thickness) and lung function. We examined differences in average lung function using mixed-effects models and differences in lung function decline using linear regression models. Current smokers were excluded. Models were adjusted for age, sex, height, weight, pack-years, socioeconomic status indicators, cohort, time, season, and weather.Measurements and Main Results: Living less than 100 m from a major roadway was associated with a 23.2 ml (95% confidence interval [CI], 244.4 to 21.9) lower FEV 1 and a 5.0 ml/yr (95% CI, 29.0 to 20.9) faster decline in FEV 1 compared with more than 400 m. Each 2 mg/m 3 increase in average of PM 2.5 was associated with a 13.5 ml (95% CI, 226.6 to 20.3) lower FEV 1 and a 2.1 ml/yr (95% CI, 24.1 to 20.2) faster decline in FEV 1 . There were similar associations with FVC. Associations with FEV 1 /FVC ratio were weak or absent.Conclusions: Long-term exposure to traffic and PM 2.5 , at relatively low levels, was associated with lower FEV 1 and FVC and an accelerated rate of lung function decline.

BackgroundHypertension is a major risk factor for cardiovascular disease and all‐cause mortality. Compared with prior guidelines, the 2017 American College of Cardiology/American Heart Association (ACC/AHA) hypertension guideline recommends lower blood pressure thresholds for defining hypertension, for initiating antihypertensive medication, and for antihypertensive medication treatment goals.Methods and ResultsTo better understand potential impacts of the 2017 guideline, we studied trends in mean systolic blood pressure and diastolic blood pressure, prevalence and burden of hypertension, and proportion of controlled hypertension in the US adult population aged ≥20 from 1999 through 2016. We used data from 38 276 adults from the National Health and Nutrition Examination Survey. Age‐standardized prevalence of hypertension decreased from 48.4% in 1999–2000 to 45.4% in 2015–2016. However, absolute burden of hypertension consistently increased, from 87.0 million in 1999–2000 to 108.2 million in 2015–2016. The age‐standardized proportion of controlled hypertension among adults receiving antihypertensive pharmacologic treatment increased from 1999–2000 (25.6%) to 2015–2016 (43.5%). There was not consistent improvement in control throughout the full period among non‐Hispanic blacks, individuals aged ≥60, or those with diabetes mellitus, chronic kidney disease, or high cardiovascular disease risk.ConclusionsBased on the 2017 guideline, from 1999 to 2016, the age‐standardized prevalence of hypertension decreased and the proportion of control among those treated for hypertension improved. However, the absolute hypertension burden increased. Among those treated, the control rate did not consistently improve in all subgroups. These data emphasize the need for continuous efforts in the prevention and control of hypertension in the US general population.

IMPORTANCE After decades of decline, the US cardiovascular disease mortality rate flattened after 2010, and racial and ethnic differences in cardiovascular disease mortality persisted.OBJECTIVE To examine 20-year trends in cardiovascular risk factors in the US population by race and ethnicity and by socioeconomic status.DESIGN, SETTING, AND PARTICIPANTS A total of 50 571 participants aged 20 years or older from the 1999-2018 National Health and Nutrition Examination Surveys, a series of cross-sectional surveys in nationally representative samples of the US population, were included.EXPOSURES Calendar year, race and ethnicity, education, and family income.MAIN OUTCOMES AND MEASURES Age-and sex-adjusted means or proportions of cardiovascular risk factors and estimated 10-year risk of atherosclerotic cardiovascular disease were calculated for each of 10 two-year cycles. RESULTSThe mean age of participants ranged from 49.0 to 51.8 years and the proportion of women from 48.2% to 51.3% in the surveys. From 1999-2000 to 2017-2018, age-and sex-adjusted mean body mass index increased from 28.0 (95% CI, 27.5-28.5) to 29.8 (95% CI, 29.2-30.4); mean hemoglobin A 1c increased from 5.4% (95% CI, 5.3%-5.5%) to 5.7% (95% CI, 5.6%-5.7%) (both P < .001 for linear trends). Mean serum total cholesterol decreased from 203.3 mg/dL (95% CI, 200.9-205.8 mg/dL) to 188.5 mg/dL (95% CI, 185.2-191.9 mg/dL); prevalence of smoking decreased from 24.8% (95% CI, 21.8%-27.7%) to 18.1% (95% CI, 15.4%-20.8%) (both P < .001 for linear trends). Mean systolic blood pressure decreased from 123.5 mm Hg (95% CI, 122.2-124.8 mm Hg) in 1999-2000 to 120.5 mm Hg (95% CI, 119.6-121.3 mm Hg) in 2009-2010, then increased to 122.8 mm Hg (95% CI, 121.7-123.8 mm Hg) in 2017-2018 (P < .001 for nonlinear trend). Age-and sex-adjusted 10-year atherosclerotic cardiovascular disease risk decreased from 7.6% (95% CI, 6.9%-8.2%) in 1999-2000 to 6.5% (95% CI, 6.1%-6.8%) in 2011-2012, then did not significantly change. Age-and sex-adjusted body mass index, systolic blood pressure, and hemoglobin A 1c were consistently higher, while total cholesterol was lower in non-Hispanic Black participants compared with non-Hispanic White participants (all P < .001 for group differences). Individuals with college or higher education or high family income had consistently lower levels of cardiovascular risk factors. The mean age-and sex-adjusted 10-year risk of atherosclerotic cardiovascular disease was significantly higher in non-Hispanic Black participants compared with non-Hispanic White participants (difference, 1.4% [95% CI, 1.0%-1.7%] in 1999-2008 and 2.0% [95% CI, 1.7%-2.4%] in [2009][2010][2011][2012][2013][2014][2015][2016][2017][2018]). This difference was attenuated (-0.3% [95% CI, -0.6% to 0.1%] in 1999-2008 and 0.7% [95% CI, 0.3%-1.0%] in 2009-2018) after further adjusting for education, income, home ownership, employment, health insurance, and access to health care. CONCLUSIONS AND RELEVANCEIn this serial cross-sectional survey study that estimated US trends in cardiovascu...

BackgroundShort‐term exposure to elevated air pollution has been associated with higher risk of acute cardiovascular diseases, with systemic oxidative stress induced by air pollution hypothesized as an important underlying mechanism. However, few community‐based studies have assessed this association.Methods and ResultsTwo thousand thirty‐five Framingham Offspring Cohort participants living within 50 km of the Harvard Boston Supersite who were not current smokers were included. We assessed circulating biomarkers of oxidative stress including blood myeloperoxidase at the seventh examination (1998–2001) and urinary creatinine‐indexed 8‐epi‐prostaglandin F2α (8‐epi‐PGF 2α) at the seventh and eighth (2005–2008) examinations. We measured fine particulate matter (PM 2.5), black carbon, sulfate, nitrogen oxides, and ozone at the Supersite and calculated 1‐, 2‐, 3‐, 5‐, and 7‐day moving averages of each pollutant. Measured myeloperoxidase and 8‐epi‐PGF 2α were loge transformed. We used linear regression models and linear mixed‐effects models with random intercepts for myeloperoxidase and indexed 8‐epi‐PGF 2α, respectively. Models were adjusted for demographic variables, individual‐ and area‐level measures of socioeconomic position, clinical and lifestyle factors, weather, and temporal trend. We found positive associations of PM 2.5 and black carbon with myeloperoxidase across multiple moving averages. Additionally, 2‐ to 7‐day moving averages of PM 2.5 and sulfate were consistently positively associated with 8‐epi‐PGF 2α. Stronger positive associations of black carbon and sulfate with myeloperoxidase were observed among participants with diabetes than in those without.ConclusionsOur community‐based investigation supports an association of select markers of ambient air pollution with circulating biomarkers of oxidative stress.